The regulation of the transcription factor nuclear factor-κB (NF-κB) during B-cell development was examined using cells isolated from the bone marrow of transgenic mice expressing a κB luciferase reporter gene. The results indicate that the highest level of NF-κB activity is present in cells expressing the pre-B-cell receptor. Furthermore, cross-linking of Igβ on CD43+ pre-B cells is able to activate NF-κB in recombination-activating gene 1-deficient mice, preceding their further differentiation into CD43- pre-B cells. Expression of a dominant negative form of IκBα using a transgenic approach or by retroviral infection leads to a reduction in the number of CD43+ pre-B cells. These data therefore indicate that activation of NF-κB in CD43+ pre-B cells, as a result of signaling by the pre-B-cell receptor, facilitates the continued development of large, CD43+ pre-B cells into small CD43- pre-B cells.
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